Y Zhang1, R-X Xu1, S Li1, C-G Zhu1, Y-L Guo1, J Sun1, J-J Li2. 1. Division of Dyslipidemia, State Key Laboratory of Cardiovascular Disease, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, BeiLiShi Road 167, Beijing 100037, China. 2. Division of Dyslipidemia, State Key Laboratory of Cardiovascular Disease, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, BeiLiShi Road 167, Beijing 100037, China. Electronic address: 13901010368@163.com.
Abstract
BACKGROUND AND AIMS: Proprotein convertase subtilisin-kexin type 9 (PCSK9) is a novel regulator of low-density lipoprotein (LDL) metabolism. Recently, small dense LDL (sdLDL) particles have been suggested to be a very atherogenic subspecies of LDL. To date, the association of sdLDL with PCSK9 is still unclear. The aim of the present study is to determine the association of sdLDL, as assayed by sdLDL-cholesterol (sdLDL-C), with PCSK9 in a cohort of subjects undergoing coronary angiography. METHODS AND RESULTS: Four hundred and ninety consecutive subjects were enrolled and classified into stable coronary artery disease (CAD) and non-CAD group. LDL separation was performed by Lipoprint System: 7 LDL subfractions were obtained and LDL score (% sdLDL) was calculated. The plasma PCSK9 levels were measured by ELISA. The data indicated that PCSK9 levels were significantly increased by sdLDL-C quartiles (p = 0.028). In age- and sex-adjusted analysis plasma sdLDL-C was positively correlated with PCSK9 levels (r = 0.157, p < 0.01). To rule out the confounding effect of dyslipidemia, we performed the analysis in subjects with and without dyslipidemia separately. Interestingly, the positive correlation of sdLDL-C with PCSK9 was only significant in patients with dyslipidemia and stable CAD (r = 0.177, p < 0.01). In a model adjusting for traditional risk factors including dyslipidemia, PCSK9 was an independent predictor of high sdLDL-C in CAD group (OR = 12.919, 95% CI 1.427-116.952) but not in non-CAD group. CONCLUSION: This study firstly demonstrated that plasma sdLDL-C was positively related to PCSK9 in patients with stable CAD, suggesting an interaction between sdLDL-C and PCSK9 in atherosclerotic coronary disease.
BACKGROUND AND AIMS: Proprotein convertase subtilisin-kexin type 9 (PCSK9) is a novel regulator of low-density lipoprotein (LDL) metabolism. Recently, small dense LDL (sdLDL) particles have been suggested to be a very atherogenic subspecies of LDL. To date, the association of sdLDL with PCSK9 is still unclear. The aim of the present study is to determine the association of sdLDL, as assayed by sdLDL-cholesterol (sdLDL-C), with PCSK9 in a cohort of subjects undergoing coronary angiography. METHODS AND RESULTS: Four hundred and ninety consecutive subjects were enrolled and classified into stable coronary artery disease (CAD) and non-CAD group. LDL separation was performed by Lipoprint System: 7 LDL subfractions were obtained and LDL score (% sdLDL) was calculated. The plasma PCSK9 levels were measured by ELISA. The data indicated that PCSK9 levels were significantly increased by sdLDL-C quartiles (p = 0.028). In age- and sex-adjusted analysis plasma sdLDL-C was positively correlated with PCSK9 levels (r = 0.157, p < 0.01). To rule out the confounding effect of dyslipidemia, we performed the analysis in subjects with and without dyslipidemia separately. Interestingly, the positive correlation of sdLDL-C with PCSK9 was only significant in patients with dyslipidemia and stable CAD (r = 0.177, p < 0.01). In a model adjusting for traditional risk factors including dyslipidemia, PCSK9 was an independent predictor of high sdLDL-C in CAD group (OR = 12.919, 95% CI 1.427-116.952) but not in non-CAD group. CONCLUSION: This study firstly demonstrated that plasma sdLDL-C was positively related to PCSK9 in patients with stable CAD, suggesting an interaction between sdLDL-C and PCSK9 in atherosclerotic coronary disease.
Authors: Julita Anna Krahel; Anna Baran; Tomasz W Kamiński; Magdalena Maciaszek; Iwona Flisiak Journal: J Clin Med Date: 2020-03-26 Impact factor: 4.241